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Acquired eyelash trichomegaly and generalized hypertrichosis associated with breast anomaly

  • Author(s): Aghaei, Shahin
  • Dastgheib, Ladan
  • et al.
Main Content

Acquired eyelash trichomegaly and generalized hypertrichosis associated with breast anomaly
Shahin Aghaei MD1, Ladan Dastgheib MD2
Dermatology Online Journal 12 (2): 19

1. Department of Dermatology, Jahrom Medical School, Jahrom, Iran. shahinaghaei@yahoo.com
2. Dermatology Clinic, Shiraz University of Medical Sciences, Shiraz, Iran


Abstract

Acquired eyelash trichomegaly is a rare condition. We present a 23-year-old woman with acquired trichomegaly and generalized hypertrichosis from childhood. The patient also exhibited bilateral nipple retraction and unilateral left-sided accessory nipple. According to our knowledge the association between trichomegaly, hypertrichosis, and breast anomaly has not been reported.



Clinical synopsis

A 23-year-old woman presented with trichomegaly and generalized hypertrichosis from childhood. At the time of first examination, bilateral nipple retraction and unilateral left-sided accessory nipple were also noted.

The patient had progressively developed both hypertrichosis and trichomegaly from age 6. The retracted breast nipples were noticed at puberty. According to her medical file, she had been hospitalized at age 12 because of aseptic meningitis. The patient never used oral medications and there is no family history of hypertrichosis or trichomegaly.

On examination, extraordinarily long eyelashes, 23 mm (Fig. 1), were observed. The eyelashes of her sibling were 10 mm long. Hypertrichosis over most of the face and torso (Figs. 2 and 5), and bilateral retracted nipples associated with left-sided accessory nipple (Figs. 3 and 4) were also noted. The scalp hair, teeth, and gingival examination were normal. There were no scars or rhytides on the face and dorsum of the hands; lymphadenopathy and organomegaly were not detected.


Figure 1Figure 2
Figure 1: The patient's acquired long lashes.
Figure 2: Facial hypertrichosis and trichomegaly.

Figure 3Figure 4
Figures 3 & 4: Hypertrichosis over the trunk associated with bilateral nipple retraction and a left-sided accessory nipple.

Figure 5
Figure 5: Hypertrichosis over the extremities.

The following laboratory examinations were within normal limits: complete blood count, erythrocyte sedimentation rate, hormonal assays (including serum testosterone, leuteinizing hormone, follicular stimulation hormone, prolactin, dihydroepiandrosterone sulfate, and thyroid function tests). Chest x-ray, breast, pelvic, and abdominal ultrasonography and ophthalmologic examination were normal. Antinuclear antibody, urine porphyrins, and fecal were negative. On chromosomal assay the patient's genotype was 46-XX. The patient has no risk factors for AIDS.


Discussion

Hypertrichosis is hair growth that is abnormal for the age, sex, or race of an individual, or for a particular area of the body [1]. One of the two major mechanisms of hypertrichosis is the conversion of vellus to terminal hairs [2]. Vellus hairs are short, nonpigmented hairs produced by follicles that penetrate only into the papillary dermis [3]. Terminal hairs are produced by follicles that penetrate to the reticular dermis; they are medullated and wider than the inner root sheath of the follicle that produces them [2].

The second major mechanism of hypertrichosis involves changes in the hair-growth cycle. Areas of the body with longer or denser hair have an increased percentage of follicles in the anagen stage or more hair follicles per unit area of skin, respectively [4]. Follicles in each body area have their own intrinsic growth pattern that may be altered by systemic influences, such as androgens, thyroid hormone, and growth hormone [5]. A less well-established mechanism of hypertrichosis is an increase in hair-follicle density [6].

Although there are a limited number of mechanisms for hypertrichosis, the triggers that initiate those mechanisms are largely unknown. Hypertrichosis is categorized as congenital or acquired, and regional (circumscribed) or generalized [7].

Several acquired disorders associated with generalized hypertrichosis are more common in childhood [1]. The major causes of acquired, generalized hypertrichosis include, cerebral disturbances (such as post viral encephalitis, head injury, and brain disorders) [8], acrodynia (chronic mercury exposure) [9], tuberculosis, malnutrition [10], AIDS [11], dermatomyositis [12], thyroid disorders [13], acquired porphyria [14], and certain drugs (such as phenytoin, cyclosporine, psoralen, diazoxide, and minoxidil) [1].

Acquired isolated trichomegaly has been reported with HIV infection [11], metastatic renal adenocarcinoma [15], dermatomyositis [16], and following treatment with cyclosporine [17] and interferon alpha-2b [18].

Severe forms of acquired hypertrichosis lanuginosa are rare. This presentation usually accompanies a serious and often fatal illness. Fine, downy hair grows over a large area of the body, replacing normal hair and primary and secondary vellus. About 60 cases have been reported and all except two were suffering from malignant disease of the gastrointestinal tract, bronchus, breast, gall bladder, or other organs [19]. One patient with lymphatic leukemia had acquired ichthyosis as well as hypertrichosis, and one had a lymphoma. The hypertrichosis may precede the diagnosis of a neoplasm by several years [20].

Our patient had no evidences of the disorders or drug consumption associated with hypertrichosis or localized trichomegaly. She had a history of aseptic meningitis during childhood that might have enhanced hypertrichosis and trichomegaly, though by history this process had begun at age 6. In addition, on physical examination she had bilateral nipple retraction and a left-sided accessory nipple. To our knowledge the association between the breast anomaly, hypertrichosis, and trichomegaly has not been reported.

Acknowledgment: The authors are very grateful to the patient who gave them written consent for this publication.

References

1. Wendelin DS, Pope DN, Mallory SB. Hypertrichosis. J Am Acad Dermatol 2003; 48: 161-79.

2. Stenn KS, Paus R. Controls of hair follicle cycling. Physiol Rev 2001; 81: 449-94.

3. Duggins OH, Trotter M. Age changes in head hair from birth to maturity: medullation in hair of children. Am J Phys Anthropol 1950; 8: 339-415.

4. Paus R, Cotsarelis G. The biology of hair follicles. N Engl J Med 1999; 341: 491-7.

5. Bertolino A, Freedberg I. Hair. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, editors. Dermatology in general medicine. New York: McGraw Hill; 1993: 671-96.

6. Cox NH, McClure JP, Hardie RA. Naevoid hypertrichosis: report of a patient with multiple lesions. Clin Exp Dermatol 1989; 14: 62-4.

7. Olsen EA. Hypertrichosis. In: Olsen EA, editor. Disorders of hair growth: diagnosis and treatment. New York: McGraw-Hill; 1993: 315-36.

8. Robinson RCV. Temporary acquired hypertrichosis following traumatic shock. Arch Dermatol 1955; 71: 401-2.

9. Dinehart SM, Dillard R, Raimer SS, Diven S, Cobos R, Pupo R. Cutaneous manifestations of acrodynia. Arch Dermatol 1988; 124: 107-9.

10. Holzel A. Hypertrichosis in childhood. Acta Paediatr Scand 1951; 40: 59-69.

11. Casanova JM, Puig T, Rubio M. Hypertrichosis in the eyelashes in acquired immunodeficiency syndrome. Arch Dermatol 1987; 123: 1599-601.

12. Reich NE, Reinhart JB. Dermatomyositis associated with hypertrichosis. Arch Dermatol Syph 1948; 57: 725-32.

13. Perloff WH. Hirsutism Ð a manifestation of juvenile hypothyroidism. JAMA 1955; 157: 651-2.

14. Cam C, Nigogosyan G. Acquired toxic porphyria cutanea tarda due to hexachlorobenzene: report of 38 cases caused by this fungicide. JAMA 1963; 183: 88.

15. Velez A, Kindelan JM, Garcia-Herola A, et al. Acquired trichomegaly and hypertrichosis in metastatic adenocarcinoma. Clin Exp Dermatol. 1995; 20(3):237-9.

16. Sharma RC, Mahajan VK, Sharma NL, et al. Trichomegaly of the eyelashes in dermatomyositis. Dermatology 2002; 205 (3):305.

17. Weaver DT, Bartley GB. CyclosporineÐ induced trichomegaly. Am J Ophthalmol. 1990; 169(2):239.

18. Hernandez- Nunez A, Fernandez Ð Herrera J, Buceta LR, et al. Trichomegaly following treatment with interferon- 2b. Lancet 2002; 359(9312):1107.

19. Hegedus SI, Schorr WF. Acquired hypertrichosis lanuginosa and malignancy. Arch Dermatol 1970; 106: 84-8.

20. Dawber RPR, de Berker D, Wojnaroska F. Disorders of hair. In: Champion RH, Burton JL, Burns DA, and Breathnach SM, editors. Textbook of Dermatology. London: Blackwell Science Ltd; 1998: 2869-2974.

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